| Project/Area Number |
23591477
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Infectious disease medicine
|
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| Research Institution | The University of Shiga Prefecture (2012-2013)
The University of Tokushima (2011) |
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Principal Investigator |
YANO mihiro 滋賀県立大学, 人間文化学部, 教授 (40304555)
|
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| Co-Investigator(Renkei-kenkyūsha) |
KIDO Hiroshi 徳島大学, 疾患酵素学研究センター, 特任教授 (50144978)
CHIDA Junji 徳島大学, 疾患酵素学研究センター, 助教 (20437651)
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| Project Period (FY) |
2011 – 2013
|
| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | インフルエンザ脳症 / エイズ脳症 / 高病原性鳥インフルエンザ / プロテアーゼ / ストレス蛋白質 |
|---|
| Research Abstract |
The vascular endothelial cell hyperpermeability seen in severe influenza is based on the disruption of adherence junctions between cells by influenza virus infection. In this study, we have shown the mechanisms of hyperpermeability of human vein endothelial cells infected with influenza A virus (PR8).The levels of beta catenin, a key regulatory component of the endothelial-cadherin cell adhesion complex, were markedly decreased during infection with increment of vascular hyperpermeability. Since the N-terminus phosphorylation of beta-catenin by GSK-3beta is the initiation step of proteasome-dependent degradation, we examined the effects of GSK-3beta suppression by RNAi. IAV infection-induced beta-catenin degradation was significantly inhibited in GSK-3beta-knockdown cells. These findings suggest that IAV infection induces GSK-3beta-mediated beta-catenin degradation in the adherence junctions and induces vascular hyperpermeability.
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